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HERC2 regulates the retention of repair proteins 53BP1, RAP80 and BRCA1 on damaged chromosomes in response to ionizing radiation by forming a complex with the ubiquitin ligases RNF8 and RNF168. Hecr2 deficiency leads to radiosensitivity.
It is unclear whether viral particles can induce membrane curvature. Binding of Simian virus 40 (SV40) to the GM1 ganglioside on host plasma membranes leads to membrane curvature and the formation of invaginations in cells and in giant unilamellar vesicles, an effect required for viral infection.
Small RNAs are known to induce heterochromatin formation in various organisms. RNA-dependent mechanisms are shown to be required for the formation of a constitutive heterochromatin structure in the chick.
The Wnt/b-catenin pathway controls proliferation and self-renewal of mouse adult neural stem cells, and the nuclear receptor TLX is shown to activate this pathway by inducing expression of Wnt7. Thus, neural stem cells promote their own self-renewal by secreting signalling molecules that act in an autocrine and paracrine mode.
During germ-cell migration in the zebrafish embryo, Rac1 and RhoA are activated at the cell front where they control formation of actin structures and retrograde flow, respectively. This is imperative for the control of E-cadherin-mediated traction forces that drive single cell migration.
DNA ligase I links newly synthesized DNA fragments. DNA ligase I deficiency causes ubiquitylation of PCNA in yeast and human by the E2 variant Mms26, Ubc47 and the E3 Rad5, which is required for activation of the DNA damage response and cell viability.
In response to CO2, leaves close their stomatal pores but the CO2-binding proteins and the cell type responsible for this effect have not been identified. Expression of β-carbonic anhydrase in guard cells modulates the CO2-mediated regulation of stomatal movements.
Cyclin-dependent kinase 2 (cdk2) is surprisingly found to suppress senescence induced by the Myc oncogene in various cell types. Inactivation or deletion of cdk2 sensitizes mouse embryonic fibroblasts to Myc-induced senescence via a mechanism requiring pRb and p53.
Shigella infection can lead to stimulation of the NF-κB pathway. IpaH9.8, a Shigella effector with ubiquitin ligase activity polyubiquitylates NEMO, a key regulator of NF-κB activation, leading to its degradation and subsequent impairment of NF-κB activation.
The molecular and cellular mechanisms that keep cells apart at compartment boundaries remain unclear. In early Drosophila embryos, cells transiently invade neighbouring compartments, but an actomyosin-based barrier formed of cable-like structures pushes them back into their compartment of origin, in mitotically active epidermis.
Exosome biogenesis is poorly understood. The small GTPases Rab27a and Rab27b and their effectors, Slp4 and Slac2b, control exosome secretion at different steps by regulating the peripheral localization, retention and docking of exosomal precursors, the multivesicular endosomes.
Mouse mutants for Sec24b, a component of COPII-coated ER-to-Golgi vesicles, have defects in convergent extension, neural tube closure and other phenotypes related to planar cell polarity (PCP). The PCP component Vangl2 is sorted by Sec24b, and Vangl2 mutants defective in convergent extension do not exit the ER.
MicroRNAs (miRNAs) regulate gene expression in many different organisms and cell types. In mouse embryonic stem cells, a regulatory circuit that involves let-7 and its target mLin41, which encodes an E3 ubiquitin ligase, facilitates polyubiquitylation of the miRNA effector Argonaute 2 (Ago2) and targets it for degradation.
During cell migration, actin retrograde flow is counteracted by integrin-mediated adhesion to the underlying matrix, providing traction for forward movement. But in the absence of this 'clutch' mechanism, some types of cells adapt their actin polymerization to maintain similar migration speeds.
Long-range communication between animal cells can be accomplished through thin tunnelling nanotubes. The generation of these delicate structures involves dynamic remodelling of actin and the plasma membrane. Now, some of the proteins that help to build these intercellular conduits have been identified.
